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Home / News / Technological Innovation / Study Finds NMN Improves Memory And Learning in Aged Rats And Eliminates Senescent Cells

Study Finds NMN Improves Memory And Learning in Aged Rats And Eliminates Senescent Cells

by: GSHWORLD Time: 2022-08-11 Classify: Technological Innovation

Recently, a research team found that NMN and lycopene have inhibitory effects on cognitive impairment in aged rats.

At the same time, NMN can improve the memory and learning ability of aged rats and eliminate senescent cells.

The combination of nicotinamide mononucleotideand lycopene prevents cognitive impairment andattenuates oxidative damage in D-galactose inducedaging models via Keap1-Nrf2 signaling


As one of the natural life processes, aging refers to the loss of reproductive capacity and the gradual decline of intrinsic physiological functions.

It is a major risk factor for various diseases, including cardiovascular disease, diabetes, and neurodegenerative diseases.

The average life expectancy has increased dramatically over the past few decades as the quality of life has improved, which has led to an increasingly aging population.

This study investigated the anti-aging effect of nicotinamide mononucleotide (NMN) and lycopene (Lyco) (NMN + Lyco) in combination on aging rats and aging PC12 cells.

In vivo and in vitro aging models were established using D-galactose (D-gal).

The combination showed a trend to outperform monotherapy in preventing aging in vivo and in vitro.

Morris water maze test showed that NMN+Lyco effectively improved the ability of spatial location learning and memory in aging model rats.

NMN + Lyco increased superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), GSH and total antioxidant capacity (T-AOC), and decreased Malondialdehyde (MDA) content.

CCK-8 assay, senescence-associated β-galactosidase staining, and flow cytometry confirmed cellular senescence in PC12 cells after D-gal exposure and indicated that NMN+Lyco has anti-aging effects in vitro.

Furthermore, NMN+Lyco effectively downregulated the expression of p53, p21 and p16 (senescence-related genes) and activated Keap1-Nrf2 signaling in both in vivo and in vitro aging models.

Collectively, NMN+Lyco protected rat and PC12 cells from D-gal-induced cognitive impairment and cellular senescence, and its effects may be related to the reduction of oxidative stress and activation of Keap1-Nrf2 signaling.

And show that NMN + Lyco has anti-aging effect in vitro.

Furthermore, NMN+Lyco effectively downregulated the expression of p53, p21 and p16 (senescence-related genes) and activated Keap1-Nrf2 signaling in both in vivo and in vitro aging models.

Collectively, NMN+Lyco protected rat and PC12 cells from D-gal-induced cognitive impairment and cellular senescence, and its effects may be related to the reduction of oxidative stress and activation of Keap1-Nrf2 signaling.

And show that NMN + Lyco has anti-aging effect in vitro.

Furthermore, NMN+Lyco effectively downregulated the expression of p53, p21 and p16 (senescence-related genes) and activated Keap1-Nrf2 signaling in both in vivo and in vitro aging models.

Collectively, NMN+Lyco protected rat and PC12 cells from D-gal-induced cognitive impairment and cellular senescence, and its effects may be related to the reduction of oxidative stress and activation of Keap1-Nrf2 signaling.

 

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